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Long term control of blood pressure
Long term control of blood pressure: Dependent on Renin angiotensin aldosterone system: This adjusts blood volume and body sodium concentration. Anatomy: New terms. Polkissen cells located between the afferent and efferent arterioles at the vascular pole of the glomerulus, adjacent to the macula densa. Their function is to measure the blood flow to the nephrons, and release renin into the blood stream if the blood pressure is low. Macula densa '''in the kidney: an area of closely packed specialized cells lining the wall of the distal tubule. The cells of the macula densa are sensitive to the concentration of sodium chloride in the distal convoluted tubule. A decrease in sodium chloride concentration initiates a signal from the macula densa that has two effects: (1) it decreases resistance to blood flow in the afferent arterioles, which increases glomerular hydrostatic pressure and helps return glomerulus filtration rate (GFR) toward normal, and (2) it increases renin release from the juxtaglomerular cells of the afferent and efferent arterioles, which are the major storage sites for renin. '''The juxtaglomerular apparatus is a microscopic structure in the kidney, which regulates the function of each nephron. The juxtaglomerular apparatus is named for its proximity to the glomerulus: it is found between the vascular pole of the renal corpuscle and the returning distal convoluted tubule of the same nephron. This location is critical to its function in regulating renal blood flow and glomerular filtration rate. The three cellular components of the apparatus are the macula densa, extraglomerular mesangial cells, and juxtaglomerular cells (juxtaglomerular cells are not granular cells but are granulated as they release Renin) The zona glomerulosa '''of the adrenal gland is the most superficial layer of the adrenal cortex, lying directly beneath the adrenal gland's capsule. Its cells are ovoid in shape and are arranged in clusters or arches (glomus is Latin for "ball"). In response to increased potassium levels, renin or decreased blood flow to the kidneys, cells of the zona glomerulosa produce and secrete the mineralocorticoid aldosterone into the blood as part of the renin-angiotensin system. Aldosterone regulates the body's concentration of electrolytes, primarily sodium and potassium, by acting on the distal convoluted tubule of kidney nephrons to: *increase sodium reabsorption *increase potassium excretion *increase water reabsorption through osmosis '''Physiology: Release of RENIN by THREE mechanisms. If blood pressure falls e.g. due to hemorrhage, perfusion to body organs decreases. Reduced renal perfusion to kidney is detected. The smooth muscle of afferent glomerular arterioles are modified to detect this. They are baroreceptors called Polkissen cells and are sensitive to stretch. When blood pressure falls, RENIN is released from these cells. When blood pressure falls, glomerular filtration rate decreases, reducing the rate of flow of fluid through the nephron. This reduced rate of flow allows more Sodium to be retained in the nephron thus decreasing the amount detected by the macula densa. In turn this stimulates them to increase renin release from the juxtaglomerular apparatus. Juxtaglomerular apparatus also has Beta 1 adrenergic receptors and these are influenced by sympathetic discharge from vasomotor center. Stimulation causes more Renin Release via neuronal mechanisms. Blood levels of Renin increase. Renin is an enzyme. In the blood already circulating there is a protein synthesized by the liver called ANGIOTENSINOGEN. It is inactive. Renin works on Angiotensinogen to convert it to Angiontensin 1 - a decapeptide. AT1 will enter the blood and enter pulmonary circulation and renal circulation. Renal and pulmonary endothelial cells secrete an enzyme called angiotensin 1 converting enzyme (ACE). This converts AT1 to Angiotensin II by removing 2 amino acids. (octapeptide). Angiotensin 1 is inactive, it exists only as a precursor. Functions of Angiotensin II. *Blood vessels have ATII receptors. ATII binding with receptors using Gq protein promotes a cascade which ultimately increases intracellular Calcium levels . (I refuse to learn this pathway! But if any want more info, go to http://en.wikipedia.org/wiki/Gq_protein). (clarifying previous two sentences) Angiotensin II through its receptor on blood vessels, uses an intracellular signaling pathway to increase calcium levels in venous and arteriolar smooth muscle. This will lead to venoconstriction and arterioloconstriction. Venoconstriction leads to increased venous return to the heart, this leads to increased END DIASTOLIC VOLUME, and this in turn leads to heart filling more, the preload increases and according to Frank Starling’s law, the stroke volume increases which means the cardiac output goes UP and leads to INCREASED SYSTOLIC PRESSURE. *Arterioloconstriction leads to increased total peripheral resistance. This leads to increased DIASTOLIC PRESSURE. *Angiotensin II has receptors in CNS: specifically on neurons in the hypothalamus. These neurons promote a sense of thirst. (it acts as a dipsogen) *Angiotensin II also directly stimulates receptors on sympathetic nerve endings. Stimulation of these receptors releases excessive amounts of nor epinephrine. This enhances sympathetic responses in the body e.g. Sympathetic stimulation of heart is increased, heart rate goes up. Blood pressure goes up. *Angiotensin II has receptors on the cells of the zona glomerulosa in the cortical area of the adrenal gland. Stimulating these cells cause them to release a lipid soluble hormone called aldosterone. *Aldosterone enters blood flow, enters renal circulation, and it affects cells called principal cells located in the kidney, which abut the collecting ducts in the distal collecting tubule of the kidney. Aldosterone changes the functioning of these principal cells in three ways. It promotes formation of more Na/K-ATPase pumps which actively push Na out of the cell and take potassium into the cell. The sodium pushed out of the principal cells ultimately end up in the blood circulation. Aldosterone also promotes formation of sodium and potassium channels on the luminal side of the principal cell. (the principal cells form alongside the glomerular tubules and the luminal side of the cell describes that side that presses up against the lumen of the glomerular tubule). These sodium channels now are used to draw sodium out of the glomerular filtrate and INTO the principal cells where it now is actively pumped OUT of the cells and ultimately into the blood circulation, taking water with them. Potassium concentrations in the principal cells increase and this diffuses OUT of the newly formed potassium channels so that the glomerular filtrate has higher concentrations of Potassium. (to put this entire point more simply: Aldosterone changes the functioning of the principal cells in the kidneys so that they absorb sodium and water from the kidneys and push them into the blood. These two factors increase blood volume, and this increases venous return, end diastolic volume, the cardiac stroke volume increases and systolic blood pressure increases. This process takes a long time, unlike the neuronal mechanism, it takes upwards of two days. Salt and water are retained and the urine has a lower volume and is high in potassium. *Angiotensin II receptors are present in the efferent arteriolar blood vessels leaving the kidney tubules in very high concentrations. ATII acting on these receptors produces vasoconstriction. By constricting the efferent arteriole, glomerular filtration is maintained, maintaining renal function. These are the long term mechanisms used by the body to maintain/control blood pressure.